Although mortality remains high in patients with acute respiratory distress syndrome (ARDS), an inflammatory lung condition, mystery remains about who develops ARDS. Pro-inflammatory (Interleukin-1beta) (IL-1beta) and anti-inflammatory (Interleukin-1 receptor antagonist) (IL-1ra) cytokine proteins influence lung injury, so the termination of genetic variations (polymorphisms) in these proteins before and after inflammatory responses might unveil which patients are most susceptible to ARDS. A quasi-experimental in vitro laboratory-based design is proposed to determine whether, in blood obtained from a convenient, anonymized sample of 140 healthy White volunteers of North American ethnic descent, cytokine protein levels of IL-1/a and IL-1ra differ before (constitutive) and after (inducible) lipopolysaccharide (LPS) stimulation), according to Interleukin-1B (IL-1B) and Interleukin-1 receptor antagonist (IL-1RN) genetic polymorphisms at specific chromosomal loci. Specific aims are to determine whether differences in constitutive and inducible cytokine protein levels are because the person carries any polymorphism, a specific polymorphism, or a combination of polymorphisms. An understanding of molecular phenomena that initiate biological inflammatory processes would offer the investigator an opportunity to learn immunologic and genetic assay techniques for genotyping and DNA microarray analysis to further study genetic susceptibility to ARDS. Cell culture supernatant from peripheral blood mononuclear cells without (constitutive) and with (inducible) LPS stimulation will be analyzed for IL-1a and IL-lra levels. Because IL-1beta may be higher during the luteal phase of the menstrual cycle, serum progesterone and 17beta-a estradiol will be analyzed in women as a potential covariate. DNA will be extracted and analyzed for IL- 1B and IL-1RN polymorphisms. Repeated measures (constitutive and inducible) of cytokine protein production (IL-1beta and IL-lra) will be analyzed according to the carrier status, chromosomal location of the polymorphism, and selected combinations of IL-1B and IL-IRN gene interactions.